The human complement system represents a severe threat for the malaria parasite Plasmodium falciparum. We previously showed that blood stage parasites bind the complement inhibitor factor H to inactivate the complement cascade. Here we investigated the potential role of plasminogen in complement evasion. Plasminogen is a zymogen of the fibrinolysis system that following processing by specific activators converts into the serine protease plasmin. Plasmin can degrade plasma proteins, including its main target fibrin and C3b. We show that the intraerythrocytic stages of P. falciparum bind plasminogen and mediate its conversion into plasmin. The protease degrades parasite-bound C3b, leading to impaired terminal complex formation. Furthermore, the acquisition of plasminogen increases parasite viability, resulting in higher parasitemia, while plasminogen-deficient serum reduces parasite growth. Our data indicate that plasminogen is acquired by the intraerythrocytic P. falciparum parasites to protect from complement-mediated lysis. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.

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